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Telomeres and Mitochondrial Metabolism: Implications for Cellular Senescence and Age-related Diseases
Open accessAbstract
Cellular senescence is an irreversible cell arrest process, which is determined by a variety of complicated mechanisms, including telomere attrition, mitochondrial dysfunction, metabolic disorders, loss of protein homeostasis, epigenetic changes, etc. Cellular senescence is causally related to the occurrence and development of age-related disease. The elderly is liable to suffer from disorders such as neurodegenerative diseases, cancer, and diabetes. Therefore, it is increasingly imperative to explore specific countermeasures for the treatment of age-related diseases. Numerous studies on humans and mice emphasize the significance of metabolic imbalance caused by short telomeres and mitochondrial damages in the onset of age-related diseases. Although the experimental data are relatively independent, more and more evidences have shown that there is mutual crosstalk between telomeres and mitochondrial metabolism in the process of cellular senescence. This review systematically discusses the relationship between telomere length, mitochondrial metabolic disorder, as well as their underlying mechanisms for cellular senescence and age-related diseases. Future studies on telomere and mitochondrial metabolism may shed light on potential therapeutic strategies for age-related diseases. Graphical Abstract The characteristics of cellular senescence mainly include mitochondrial dysfunction and telomere attrition. Mitochondrial dysfunction will cause mitochondrial metabolic disorders, including decreased ATP production, increased ROS production, as well as enhanced cellular apoptosis. While oxidative stress reaction to produce ROS, leads to DNA damage, and eventually influences telomere length. Under the stimulation of oxidative stress, telomerase catalytic subunit TERT mainly plays an inhibitory role on oxidative stress, reduces the production of ROS and protects telomere function. Concurrently, mitochondrial dysfunction and telomere attrition eventually induce a range of age-related diseases, such as T2DM, osteoporosis, AD, etc. :increase; :reduce;⟝:inhibition.
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“persistent DDR activation at telomeres, the ends of chromosomes, which is sufficient to activate replicative cell senescence [8]”
From The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence (2022) · cites this paper as [8]
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“oncogene activation partly via reactive oxygen species (ROS) production, determining hyperproliferation and altered DNA replication profiles [4,8]”
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Metadata
- Authors
- Gao, X., Yu, X., Zhang, C., Wang, Y., Sun, Y., Sun, H., Zhang, H., Shi, Y., & He, X.
- Affiliations
- Jilin University (CN)
- Corresponding author
- He, Xu
- Venue
- Stem Cell Reviews and Reports
- Published
- 2022-04-23
- Volume
- 18
- Issue
- 7
- Pages
- 2315-2327
- ISSN
- 1550-8943 (ISSN-L)
- 2629-3269
- 2629-3277
- PMC
- PMC9033418
- OpenAlex
- W4224234800
- Cited by
- 180
- References
- 108
- Citations by year
- 2026: 41 · 2025: 61 · 2024: 41 · 2023: 32 · 2022: 5
- FWCI
- 4.78
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Stem Cell Reviews and Reports (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Science and Technology Projects of the Education Department of Jilin Province (JJKH20221058KJ)
- Scientific Research Project of Jilin Provincial Bureau of Health (2020J030)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Keywords
- cellular senescence, telomere shortening, mitochondrial dysfunction, mitochondrial metabolism, age-related diseases, oxidative stress, reactive oxygen species, telomerase reverse transcriptase (TERT), DNA damage, neurodegenerative diseases, type 2 diabetes, osteoporosis, metabolic imbalance, apoptosis
- MeSH terms
- Adenosine Triphosphate, Aged, Aging, Animals, Humans, Mitochondria, Telomere, Cellular Senescence, Reactive Oxygen Species, Telomerase, Mice
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